Abstract
The relative rate of calcium transport into platelets from essential hypertensive patients and healthy normotensive donors was measured using the metallochromic indicator arsenazo III and recording net decrease in optical density per 5 minutes (O.D.U./ 5 min). When platelets from essential hypertensive patients were suspended in the patient's own serum, calcium was transported more rapidly than when suspended in normal sera (0.0166 vs 0.0113 O.D.U./ 5 min, P < 0.01) indicating that the difference is due to a circulating factor. When platelets from healthy normotensive volunteers were suspended in the donor's own serum or in a pool of normal sera, the relative rate of transport was lower than in the case of platelets from hypertensives suspended in the pool of normal sera (0.005 vs 0.0113 O.D.U./ 5 min, P < 0.01) which suggests a membrane alteration rendering the platelets from hypertensives more permeable to calcium. It was observed that the increase of calcium entry was inhibited by verapamil.
The nature of these circulating and membrane-associated factors is at present unknown, but the circulating factor was capable of increasing the membrane permeability to calcium in normal human platelets (from 0.0057 to 0.011 O.D.U./5 min, P < 0.01) and even in rat liver mitochondria, an effect that was inhibited by ruthenium red.